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Libros sobre el tema "Thr protein phosphatases"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 1 de febrero de 2022

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1

International Conference on Second Messengers and Phosphoproteins (12th 2004 Montréal, Québec). Second messengers and phosphoprotein signaling: Proceedings of the 12th International Conference on Second Messengers and Phosphoproteins : Montreal, Canada, August 3-7, 2004. Editado por Anand-Srivastava Madhu B, Tremblay Michel y Srivastava Ashok K. Bologna: Medimond International Proceedings, 2004.

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2

Yuen, Kenneth Wing Hon. Analyses of the roles of protein tyrosine phosphatase SHP-2 and SLAM-associated protein (SAP) in regulation of T cell functions. Ottawa: National Library of Canada, 2002.

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3

Swain, James Edward. The effects of okaidic acid, a protein phosphatase inhibitor, on synaptic transmission at the crayfish neuromuscular junction. Ottawa: National Library of Canada, 1990.

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4

Tsiani, Evangelia. Regulation of metabolic effects in L6 muscle cells by sulfonylureas and the protein tyrosine phosphatase inhibitors vanadate and pervanadate. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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5

Hoof, C. Van. Prpa - a Protein Controlling the Dual Specificity of Protein Phosphatase. Leuven University Press, 1994.

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6

Waelkens, E. Regulation and Specificity of the Polycation-Stimulated Protein Phosphatases. Leuven University Press, 1988.

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7

Janssens, Veerle. Promoter Analysis and Characterization of Novel Splice Variants of the Human Phosphotyrosyl Phosphatase Activator Gene. Leuven Univ Pr, 2000.

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8

Jagiello, I. The Structure and Regulation of Protein Phosphatase-1 in the Nucleus. Leuven University Press, 1998.

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9

Wera, S. Purification and Characterisation of the Glycogen-Bound Protein Phosphatase from Rat Liver. Leuven University Press, 1991.

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10

Bollen, M. The Structure and Regulation of Type-1 Protein Phosphatases Involved in Hepatic Glycogen Metabolism. Leuven University Press, 1991.

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11

Boudrez, an. Interaction of the Protein Phosphatase-1 Regulator Nipp1 With Pre-Mrna Splicing Factors. Leuven Univ Pr, 2002.

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12

Hum, Gabriel. Novel approaches towards the synthesis of protein tyrosine phosphatase inhibitors and alternative strategies in the design of transition state analogues for phosphatase abzymes. 2002.

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13

Batt, Jane. Characterization of the role of protein tyrosine phosphatase sigma (PTP[sigma]) in mammalian development. 2002.

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14

Sorby, Maria. Structural and Functional Studies of the Density Enhanced Receptor-Like Protein Tyrosine Phosphatase Dep-1. Uppsala Universitet, 2001.

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15

Kotoris, Christopher C. The synthesis of novel organofluorines by electrophilic fluorination and their evaluation as inhibitors of protein tyrosine phosphatase 1B. Dept of Chemistry, U of Toronto, 2000.

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16

Menon, Deepa U. Autism and Intellectual Disabilities. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0053.

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PTEN (phosphatase and tensin homologue) on chromosome 10q23.3 is a tumor suppressor gene that encodes for a dual specificity phosphatase that regulates the phosphatidylinositol 3- kinase pathway and has an important role in brain development by affecting neuronal survival, neurite outgrowth, synaptic plasticity, and learning memory. Germline mutations of the PTEN gene have been implicated in a group of related tumor syndromes with autosomal dominant inheritance and variable expression and include the Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome, Proteus syndrome, and Juvenile Polyposis syndrome. These syndromes are collectively called the PTEN hamartoma tumor syndromes (PHTS) because they have a predisposition to tumors and hamartomas. PTEN germ line mutations have also been recently linked to autism and macrocephaly and the prevalence of PTEN mutation in children with autism spectrum disorder, and macrocephaly is reported to range from 1.1% to 16.7%.

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17

Winter, Sherry Lynn. Genetic and functional characterization of the interaction of BRCA1 with the serine/threonine phosphatase, PP1, and the circadian clock proteins, Per1 and Per2. 2006.

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18

Abhishek, Abhishek y Michael Doherty. Pathophysiology of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0049.

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Calcium pyrophosphate (CPP) dihydrate crystals form extracellularly. Their formation requires sufficient extracellular inorganic pyrophosphate (ePPi), calcium, and pro-nucleating factors. As inorganic pyrophosphate (PPi) cannot cross cell membranes passively due to its large size, ePPi results either from hydrolysis of extracellular ATP by the enzyme ectonucleotide pyrophosphatase/phosphodiesterase 1 (also known as plasma cell membrane glycoprotein 1) or from the transcellular transport of PPi by ANKH. ePPi is hydrolyzed to phosphate (Pi) by tissue non-specific alkaline phosphatase. The level of extracellular PPi and Pi is tightly regulated by several interlinked feedback mechanisms and growth factors. The relative concentration of Pi and PPi determines whether CPP or hydroxyapatite crystal is formed, with low Pi/PPi ratio resulting in CPP crystal formation, while a high Pi/PPi ratio promotes basic calcium phosphate crystal formation. CPP crystals are deposited in the cartilage matrix (preferentially in the middle layer) or in areas of chondroid metaplasia. Hypertrophic chondrocytes and specific cartilage matrix changes (e.g. high levels of dermatan sulfate and S-100 protein) are related to CPP crystal deposition and growth. CPP crystals cause inflammation by engaging with the NALP3 inflammasome, and with other components of the innate immune system, and is marked with a prolonged neutrophilic inflitrate. The pathogenesis of resolution of CPP crystal-induced inflammation is not well understood.

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19

Voinescu, Alexandra, Nadia Wasi Iqbal y Kevin J. Martin. Management of chronic kidney disease-mineral and bone disorder. Editado por David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0118_update_001.

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In all patients with chronic kidney disease (CKD) stages 3–5, regular monitoring of serum markers of CKD-mineral and bone disorder, including calcium (Ca), phosphorus (P), parathyroid hormone (PTH), 25-hydroxyvitamin D, and alkaline phosphatase, is recommended. Target ranges for these markers are endorsed by guidelines. The principles of therapy for secondary hyperparathyroidism include control of hyperphosphataemia, correction of hypocalcaemia, use of vitamin D sterols, use of calcimimetics, and parathyroidectomy. of hyperphosphataemia is crucial and may be achieved by means of dietary P restriction, use of P binders, and P removal by dialysis. Dietary P restriction requires caution, as it may be associated with protein malnutrition. Aluminium salts are effective P binders, but they are not recommended for long-term use, as Aluminium toxicity (though from contaminated dialysis water rather than oral intake) may cause cognitive impairment, osteomalacia, refractory microcytic anaemia, and myopathy. Ca-based P binders are also quite effective, but should be avoided in patients with hypercalcaemia, vascular calcifications, or persistently low PTH levels. Non-aluminium, non-Ca binders, like sevelamer and lanthanum carbonate, may be more adequate for such patients; however, they are expensive and may have several side effects. Furthermore, comparative trials have failed so far to provide conclusive evidence on the superiority of these newer P binders over Ca-based binders in terms of preventing vascular calcifications, bone abnormalities, and mortality. P removal is about 1800–2700 mg per week with conventional thrice-weekly haemodialysis, but may be increased by using haemodiafiltration or intensified regimens, such as short daily, extended daily or three times weekly nocturnal haemodialysis. Several vitamin D derivatives are currently used for the treatment of secondary hyperparathyroidism. In comparison with the natural form calcitriol, the vitamin D analogue paricalcitol seems to be more fast-acting and less prone to induce hypercalcaemia and hyperphosphataemia, but whether these advantages translate into better clinical outcomes is unknown. Calcimimetics such as cinacalcet can significantly reduce PTH, Ca, and P levels, but they have failed to definitively prove any benefits in terms of mortality and cardiovascular events in dialysis patients. Parathyroidectomy is often indicated in CKD patients with severe persistent hyperparathyroidism, refractory to aggressive medical treatment with vitamin D analogues and/or calcimimetics. This procedure usually leads to rapid improvements in biochemical markers (i.e. significant lowering of serum Ca, P, and PTH) and clinical manifestations (such as pruritus and bone pain); however, the long-term benefits are still unclear.

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